Objective To investigate genes involved in the mechanisms underlying the progression of severe preeclampsia.Methods We conducted a muhiregional gene expression analysis using peripheral leucocytes from patients with preeclampsia and normal controls.Total RNA was extracted from peripheral blood of six severe preeclampsia and five normotensive pregnancies.We performed genome-wide expression profiling using Affymetrix HG_U133 plus 2.0 chips to screen out differentially expressed genes of 2 fold or more and q_value ＜ 5.4%.Using Gene Ontology we identified the function of differentially expressed genes after cluster analysis.Results Among the 47 000 genes that were screened in the microarray,140 genes were found to be differentially expressed between normal and preeclamptic pregnancies. Eighty six up-regulated candidate genes were mainly involved in cysteine metabolism urea cycle and metabolism of amiogroups,proteasome,TGF-beta signaling pathway, and the ratio of calponin2 (CNN2), matrix metallopeptidase 8 (MMP8),V-set and immunoglobulin domain containing 4 (VSIG4),proteasome 26S subunit ATPase 5 (PSMC5) was evidently increased in preeclampsia patients.Among 54 down-regulatedcandidates,natural killer cell mediated cytotoxicity,antigen processing and presentation,metabolism of xenobiotics by cytochrome P450 were the main pathways.KIR3DL2,AKR1C3,CHURC1 and SLC25A13 were obviously decreased in preeclampsia patients. Conclusions The gene expression of peripheral leucocytes in preeclampsia patients is significantly different from that of uncomplicated pregnancies.CNN2,MMP8,VSIG4,PSMC5,KIR3DL2,AKR1C3,CHURC1 and SLC25A13 may be involved in the molecular mechanisms underlying the progression of severe preeclampsia.

Objective To study any protection against hippocampal neuron damage induced by epilepsy (SE) provided by transcutaneous stimulation (TNS) of the trigeminal nerve and to document any effect of such stimulation on the expression of glutamic acid decarboxylase (GAD) 65/67.Methods Pilocarpine injection was used to induce epilepsy in healthy male Sprague-Dawley rats which were then randomly divided into a treatment group and a model group.Rats which had not received the pilocarpine injection served as normal controls.In the treatment group the rats were given electrostimulation for one month after the first spontaneous seizure following the injection of pilocarpine.In the model group they were given sham TNS for one month.After the month of stimula-tion,immunohistochemistry was used to detect the expression of GAD65/67 in the hippocampus.Terminal deoxy-nucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assays and Nissl staining were applied to deter-mine apoptosis and neuron loss in the hippocampus.Results Significantly less apoptosis was observed in the treatment group than in model group at 24 h,48 h and 72 h post-injection.Compared to the model group,average GAD65/67 expression had increased significantly in the treatment group at 24 h,72 h,1 week,2 weeks and 4 weeks post-stimulation.GAD65 expression reached its peak from 72 h to 1 week post-stimulation,then decreased to the level of the control group by 4 weeks post-stimulation.The expression of GAD67 remained elevated at all the time points employed.Conclusions TNS can significantly protect hippocampal neurons from damage in epilepsy,at least in rats.The underlying anti-epileptic and neuroprotective mechanisms may involve increased inhibitory transmission induced by the stimulation.

Objective To study the main risk factors related to the incidence of tuberculosis in China and to provide di -rections and basis for the protection of tuberculosis .Methods The results of 25 studies on the main risk factors of tubercu-losis of Chinese people from 2000 to 2012 were analyzed by meta-analysis method .Results The pooled odds radio values and 95%CI of history of exposure to pulmonary tuberculosis , smoking, marriage, contact with people, Bacille Calmette-Guerin (BCG)vaccination scar, BCG vaccination, low body mass index(BMI) , family history of tuberculosis, exposure to dust and to chemical fumes under working conditions were as follows:3.14(2.74-3.59),1.23(1.14 -1.33),3.05 (2.10-4.45),2.08(1.76-2.26),0.39(0.32 -0.47),0.58(0.46 -0.73),2.95(2.40 -3.64),2.56(1.82 -3.59),2.58(2.04-3.26),and 4.81(1.99-11.60).Conclusion Then History of exposure to pulmonary tuberculosis , smoking, marriage, contact with people , low BMI, family history of tuberculosis , exposure to dust and to chemical fumes under working conditions are considered to be the risk factors of pulmonary tuberculosis .While BCG vaccination scar and BCG vaccination are considered to be the protective factors of pulmonary tuberculosis .

Objective:To explore the application effect of modified early cardiac rehabilitation in patients with acute myocardial infarction after percutaneous coronary intervention (PCI) .Methods:Using the convenient sampling method, a total of 193 patients who were diagnosed with acute ST-segment elevation myocardial infarction and underwent PCI in Huabei Petroleum Administration Bureau General Hospital were selected as research objects from January 2018 to January 2020. They were randomly divided into the observation group (97 cases) and the control group (96 cases) . Patients in the control group received routine nursing, while the observation group received modified early cardiac rehabilitation nursing. The Barthel Index, 6-Minute Walk Test (6MWT) and the MOS Item Short from Health Survey (SF-36) were used to compare the effects of interventions.Results:After intervention, the distance of 6MWT in the observation group was longer than that in the control group, and the score of Barthel Index in the observation group was higher than that in the control group, and the differences were statistically significant ( P<0.05) . After 6 months of follow-up, scores of general health, social function, emotional function, physiological function and mental health in SF-36 of the observation group were higher than those of the control group, and the differences were statistically significant ( P<0.05) . Conclusions:Modified early cardiac rehabilitation is beneficial to improve the activity of daily living, increase exercise tolerance and improve quality of life of patients with acute myocardial infarction after PCI.

Objective The study was to investigate the activation of tumor necrosis factor α (TNF-α) mRNA transcription and protein expression in peripheral blood and activation of signal path PI3K/AKT in patients with chronic heart failure. Methods From February 2015 to April 2018, 244 patients with heart failure in the cardiovascular department of our hospital were selected as heart failure group, while 244 healthy cases were enrolled as the control group at the same time. The peripheral blood samples of two groups were collected. We detected the transcription and protein expression of TNF-α mRNA and the activation of PI3K, AKT in peripheral blood. The left ventricular ejection fraction (LVEF) were measured in two groups. The correlations between influencing factors and LVEF were analyzed. Results The levels of PI3K, AKT in the heart failure group were higher than those in the control group. The differences were statistically significant respectively (P < 0.05). The mRNA relative content and protein content of TNF-α in peripheral blood mononuclear cells of heart failure group were higher compared with those of control group (P < 0.05). The LVEF of heart failure group was significantly lower than that of the control group (34.50 ± 6.33) ％ versus (55.60 ± 2.49) ％, P < 0.001). Among 244 patients with heart failure, Spearman correlation analysis showed that there were significant positive correlations between TNF-a mRNA and protein expression levels and the levels of PI3K, AKT respectively (P < 0.05). Multiple factors unconditional Logistic regression analysis showed that the TNF-α mRNA, protein expression and PI3K, AKT levels in peripheral blood were independent risk factors for LVEF (P < 0.05). Conclusion The expression levels of PI3K, AKT and TNF-α are all significantly increased in chronic heart failure patients, which could participate in the occurrence and development of heart failure.

Objective:To retrieve, evaluate and summarize the evidence of perioperative delirium prevention and care in elderly patients with fractures, and provide a basis for standardized prevention, care and management in clinical practice.Methods:The evidence was systematically retrieved from the Guidelines International Network, National Guidelines Library, Institute for Healthcare Optimization, UpToDate, BMJ Best Practice, Joanna Briggs Institute Center for Evidence Based Health Care, Cochrane Library, Yimaitong, CINAHL, Embase, BMJ, PubMed, CNKI , Wanfang, and China Biology Medicine disc (CBMdisc) , including guidelines, evidence summary, systematic reviews, best practice information, and randomized controlled trials (RCT) published up to December 1, 2019.Results:Finally, 15 articles were included, including 2 clinical decision-making, 5 guidelines, 5 systematic reviews, 2 summaries of evidence, and 1 RCT. The best evidence included 11 aspects such as delirium risk factor assessment, assessment tools, assessment timing, and qualifications of assessors, with a total of 25 pieces of evidence.Conclusions:Perioperative delirium in elderly patients with fractures has not yet gained the full attention from healthcare professionals. Medical institutions should establish standardized procedures for the evaluation, prevention, and care of elderly patients with fractures based on evidence-based evidence transformation, improve the health education system for medical staff and patients, formulate corresponding norms, improve the level of delirium care, and improve patients' outcomes.

Tolerogenic dendritic cells (tolDCs) facilitate the suppression of autoimmune responses by differentiating regulatory T cells (Treg). The dysfunction of immunotolerance results in the development of autoimmune diseases, such as rheumatoid arthritis (RA). As multipotent progenitor cells, mesenchymal stem cells (MSCs), can regulate dendritic cells (DCs) to restore their immunosuppressive function and prevent disease development. However, the underlying mechanisms of MSCs in regulating DCs still need to be better defined. Simultaneously, the delivery system for MSCs also influences their function. Herein, MSCs are encapsulated in alginate hydrogel to improve cell survival and retention in situ, maximizing efficacy in vivo. The three-dimensional co-culture of encapsulated MSCs with DCs demonstrates that MSCs can inhibit the maturation of DCs and the secretion of pro-inflammatory cytokines. In the collagen-induced arthritis (CIA) mice model, alginate hydrogel encapsulated MSCs induce a significantly higher expression of CD39⁺CD73⁺ on MSCs. These enzymes hydrolyze ATP to adenosine and activate A_2A/2B receptors on immature DCs, further promoting the phenotypic transformation of DCs to tolDCs and regulating naïve T cells to Tregs. Therefore, encapsulated MSCs obviously alleviate the inflammatory response and prevent CIA progression. This finding clarifies the mechanism of MSCs-DCs crosstalk in eliciting the immunosuppression effect and provides insights into hydrogel-promoted stem cell therapy for autoimmune diseases.

Monocytes are key effectors in autoimmunity-related diseases in the central nervous system (CNS) due to the critical roles of these cells in the production of proinflammatory cytokines, differentiation of T-helper (Th) cells, and antigen presentation. The JAK-STAT signaling is crucial for initiating monocytes induced immune responses by relaying cytokines signaling. However, the role of this pathway in modulating the communication between monocytes and Th cells in the pathogenesis of multiple sclerosis (MS) is unclear. Here, we show that the JAK1/2/3 and STAT1/3/5/6 subtypes involved in the demyelination mediated by the differentiation of pathological Th1 and Th17 and the CNS-infiltrating inflammatory monocytes in experimental autoimmune encephalomyelitis (EAE), a model for MS. JAK inhibition prevented the CNS-infiltrating CCR2-dependent Ly6C^hi monocytes and monocyte-derived dendritic cells in EAE mice. In parallel, the proportion of GM-CSF⁺CD4⁺ T cells and GM-CSF secretion were decreased in pathological Th17 cells by JAK inhibition, which in turns converted CNS-invading monocytes into antigen-presenting cells to mediate tissue damage. Together, our data highlight the therapeutic potential of JAK inhibition in treating EAE by blocking the GM-CSF-driven inflammatory signature of monocytes.